IVMS-CV-Basic Electrocardiography Notes

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Basic Electrocardiography
Link to Companion Power Point Presentation

Objectives

Given a standard EKG, the student should be able to:

 Determine the rate
 Determine that the rhythm is regular or irregular
 Determine the PQRST intervals
 Determine the axis
 Determine whether atrial enlargement exists
 Determine whether ventricular hypertrophy exists
 Determine the presence or absence of infarction or ischemia

General Principles and Definitions

Depolarization: Electrical activation of the myocardium.

Repolarization: Restoration of the electrical potential of the myocardial cell.

Sequence: Depolarization occurs in the sinoatrial (SA) node; current travels
through internodal tracts of the atria to the atrioventricular (AV) node; then
through Bundle of His, which divides into right and left bundle branches; left
bundle branch divides into left anterior and posterior fascicles.

ECG: A galvanometer and electrodes with six limb leads and six chest leads.
Gives a graphic recording of the electric forces generated by the heart during
depolarization and repolarization. The electrocardiogram is recorded on graph
paper with divisions.

Marc Imhotep Cray, M.D.

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http://upload.wikimedia.org/wikipedia/commons/c/c1/ECGcolor.svg


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P wave: ECG deflection representing atrial depolarization. Atrial repolarization
occurs during ventricular depolarization and is obscured.

QRS wave: ECG deflection representing ventricular depolarization.

T wave: ECG defection representing ventricular repolarization.

ECG Electrodes: Two arrangements, bipolar and unipolar leads.

Bipolar Lead: One in which the electrical activity at one electrode is compared
with that of another. By convention, a positive electrode is one in which the ECG
records a positive (upward) deflection when the electrical impulse flows toward it
and a negative (downward) deflection when it flows away from it.

Unipolar Lead: One in which the electrical potential at an exploring electrode is
compared to a reference point that averages electrical activity, rather than to that
of another electrode. This single electrode, termed the exploring electrode, is the
positive electrode.

Limb Leads: I, II, III, aVR, aVL, aVF explore the electrical activity in the heart in
a frontal plane; i.e., the orientation of the heart seen when looking directly at the
anterior chest.

Standard Limb Leads: I, II, III; bipolar, form a set of axes 60° apart

Lead I: Composed of negative electrode on the right arm and positive electrode
on the left arm.

Lead II: Composed of negative electrode on the right arm and positive electrode
on the left leg.

Lead III: Composed of negative electrode on the left arm and positive electrode
on the left leg.

Augmented Voltage Leads: aVR, aVL aVF; unipolar ; form a set of axes 60°
apart but are rotated 30° from the axes of the standard limb leads.

aVR: Exploring electrode located at the right shoulder.

aVL: Exploring electrode located at the left shoulder.


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aVF: Exploring electrode located at the left foot.

Reference Point for Augmented Leads: The opposing standard limb lead; i.e.,
that standard limb lead whose axis is perpendicular to the particular augmented
lead.

Chest Leads: Vl, V2, V3, V4, V5, V6, explore the electrical activity of the heart in
the horizontal plane; i.e., as if looking down on a cross section of the body at the
level of the heart. These are exploring leads.

Reference Point for Chest Leads: The point obtained by connecting the left
arm, right arm, and left leg electrodes together.

Vl: Positioned in the 4th intercostal space just to the right of the sternum.

V2: Positioned in the 4th intercostal space just to the left of the sternum.

V3: Positioned halfway between V2 and V4.

V4: Positioned at the 5th intercostal space in the mid-clavicular line.

V5: Positioned in the anterior axillary line at the same level as V4.

V6: Positioned in the mid axillary line at the same level as V4 and V5.

Vl and V2*: Monitor electrical activity of the heart from the anterior aspect,
septum, and right ventricle.


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V3 and V4*: Monitor electrical activity of the heart from the anterior aspect.

V5 and V6*: Monitor electrical activity of the heart from the left ventricle and
lateral aspect.

Normal R Wave Progression: Vl Consists of a small R wave and a large S
wave, whereas V6 consists of a small Q wave and a large R wave. Since V3 and
V4 are located midway between Vl and V6, the QRS complex would be expected
to be nearly isoelectric in one of these leads; i.e., the positive and negative
deflections will be about equal.

Normal ECG:

 Pulse rate lies between 60 and 100 beats/minute

 Rhythm is regular except for minor variations with respiration.

 P-R interval is the time required for completion of aerial depolarization;
conduction through the AV note, bundle of His, and bundle branches; and
arrival at the ventricular myocardial cells. The normal P-R interval is 0 12
to 0.20 seconds.

 The QRS interval represents the time required for ventricular cells to
depolarize. The normal duration is 0.06 to 0.10 seconds.

 The Q-T interval is the time required for depolarization and repolarization
of the ventricles.

The time required is proportional to the heart rate. The faster the heart rate, the
faster the repolarization, and therefore the shorter the Q-T interval. With slow
heart rates, the Q-T interval is longer. The Q-T interval represents about 40% of
the total time between the QRS complexes (the R-R interval). In most cases, the
Q-T interval lasts between 0.34 and 0.42 seconds.

Dimensions of Grids on ECG Paper: Horizontal axis represents time. Large
blocks are 0.2 seconds in duration, while small blocks are 0.04 seconds in
duration. Vertical axis represents voltage. Large blocks are 5mm, while small
blocks represent 1mm.


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Estimation of Heart Rate

Heart Rates of 50 to 300 beats/min.: Can be estimated from the number of
large squares in an R-R interval. Because there are 300 large blocks in one
minute, the number of blocks between R-R intervals can be divided into 300 to
approximate the rate. For example, one large block between R-R intervals would
be determined thusly:

Heart Rates of <50 beats/minute: Can be estimated with the aid of markings at
3-second intervals along the graph paper. To calculate the rate, the cycles on a
6-second interval (two 3-second markings) are multiplied by 10 (to give the rate
per 60 seconds; i.e., per minute).

Sinus Rhythm Disturbances

Background: Sinus rhythms originate in the sinoatrial node. Diagnosis of sinus
rhythms requires examining leads II and aVR for the correct polarity of the P
waves. The P wave is always positive in lead II and negative in lead aVR. A P
wave will precede each QRS complex, and the P-R interval should be constant.

Sinus Tachycardia: Sinus rhythm with a rate >100 beats per minute. With fast
rates, P waves may merge with preceding T waves and be indistinct. Can
originate from the sinoatrial node, atrial muscle, or atrioventricular junction. Often
referred to as supraventricular tachycardia without specifying site of origin.


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Sinus Bradycardia: Sinus rhythm with a rate <60 beats per minute

Sinoatrial Block: Refers to failure of the sinus node to function for one or more
beats. In this condition, there are simply one or more missing beats; i. e., there
are no P waves or QRS complexes seen. Fortunately, when the sinus fails to
function for a significant period of time (sinus arrest), another part of the
conduction system usually assumes the role of pacemaker. These pacing beats
are referred to as escape beats and may come from the atria, the atrioventricular
junction, or the ventricles.

Sick Sinus Syndrome: In elderly people, the sinus node may undergo
degenerative changes and fail to function effectively. Periods of sinus arrest,
sinus tachycardia, or sinus bradycardia may occur.

Atrial Arrhythmias

Background: Include premature atrial beats, paroxysmal atrial tachycardia,
multi-focal atrial tachycardia, atrial flutter, and atrial fibrillation. Because the
stimuli arise above the level of the ventricles, the QRS pattern usually is normal.

Premature Atrial Contraction (PAC): An ectopic beat arising somewhere in
either atrium but not in the sinoatrial node. Occurs before the next normal beat is
due, and a slight pause usually follows. The P wave may have a configuration
different from the normal P wave and may even be of opposite polarity.

Occasionally, the P wave will not be seen because it is lost in the preceding T
wave. The P-R interval may be shorter then the normal. If the premature atrial
depolarization wave reaches the AV node before the node has had a chance to
repolarize, it may not be conducted, and what may be seen is an abnormal P
wave without a subsequent QRS complex. These premature atrial depolarization
waves may be conducted to ventricular tissue before complete repolarization has
occurred, and in such cases, the subsequent ventricular depolarization may take
place by an abnormal pathway, generating a wide, bizarre QRS complex.

Paroxysmal Atrial Tachycardia (PAT): Defined as three or more consecutive
PACs. PAT usually occurs at a regular rate, most commonly between 150 and
250 beats per minute. P waves may or may not be seen and may be difficult to
differentiate from sinus tachycardia.

Multi-Focal Atrial Tachycardia (MFAT): Results from the presence of multiple,
different atrial pacemaker foci. This rhythm disturbance is characterized by a
tachycardia with beat-to-beat variation of the P wave morphology.

Atrial Flutter: An ectopic atrial rhythm. Instead of P waves, characteristic
sawtooth waves are seen. The atrial rate in atrial flutter is usually about 300
beats per minute. However, the AV junction is unable to contract at this rapid rate,

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so the ventricular rate is less-usually 150, 100, 75, and so on, beats per minute.
Atrial flutter with a ventricular rate of 150 beats per minute is called a two-for-one
flutter because of the ratio of the atrial rate (300) to the ventricular rate (150).

Atrial Fibrillation: Here the atria are depolarized at an extremely rapid rate,
greater then 400 beats per minute. This produces a characteristic wavy baseline
pattern instead of normal P waves. Because the AV junction is refractory to most
of the impulses reaching it, it only allows a fraction of them to reach the ventricles.
The ventricular rate, therefore, is only 110-180 beats per minute. Also
characteristic of atrial fibrillation is a haphazardly irregular ventricular rhythm.

Junctional Rhythms

Background: The three types of junctional rhythms are premature junctional
contractions, junctional tachycardia, and junctional escape rhythms. Junctional
rhythms arise in the AV junction. P waves, when seen, are opposite their normal
polarity. They are called retrograde P waves. These P waves may precede, be
buried in, or follow the QRS complex. Since the stimulus arises above the level of
the ventricles, the QRS complex is usually of normal configuration.

Premature Junctional Contractions: Can occur since the AV junction may also
serve as an ectopic pacemaker. These are similar to PACs, in that they occur
before the next beat is due and a slight pause follows the premature beat.

Atrioventricular Junctional Tachycardia: A run of 3 or more premature
junctional beats. Has about the same rate as PAT and often cannot be
distinguished from it. The difference is not clinically significant.

Atrioventricular Junctional Escape Beat: An escape beat that occurs after a
pause in the normal sinus rhythm. Atrial pacing usually resumes after the
junctional beat. A junctional escape rhythm, defined as a consecutive run of
atrioventricular junctional beats, may develop if the SA node does not resume the
pacemaker role. Junctional escape rhythm has a rate between 40 and 60 beats
per minute.


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Atrioventricular Heart Blocks

Background: Heart block occurs in 3 forms: first degree. second degree, and
third degree. Second degree heart block is divided into two types: Mobitz type 1
and Mobitz type 2.

First Degree Heart Block: The ECG abnormality is simply a prolonged P-R
interval to greater than 0.2 seconds.

Second Degree Heart Block, Mobitz Type 1: The characteristic ECG is
progressive lengthening of the P-R interval until finally a beat is dropped. The
dropped beat is seen as a P wave that is not followed by a QRS complex.

Second Degree Heart Block, Mobitz Type 2: A more severe form of second
degree block, since it often progresses to complete heart block. The
characteristic ECG picture is that of a series of non-conducted P waves; e.g., 2:1,
3:1, 4:1, block.

Third Degree Heart Block: Also known as: Complete Heart Block. The
atrioventricular junction does not conduct any stimuli from the atria to the
ventricles. Instead, the atria and the ventricles are paced independently. The
characteristic ECG picture is: (1) P waves are present and occur at a rate faster
than the ventricular rate; (2) QRS complexes are present and occur at a regular
rate, usually <60 beats per minute; and (3) the P waves bear no relationship to
the QRS complexes. Thus, the P-R intervals are completely variable. The QRS
complex may be of normal or abnormal width, depending on the location of the
blockage in the AV junction.

Pre-Excitation Syndromes

Background: Pre-excitation syndromes refer to clinical Conditions in which the
wave of depolarization bypasses the atrioventricular node as it passes from the
atria to the ventricles. The time required for the wave to leave the sinoatrial node
and arrive at ventricular muscle (P-R interval) is, therefore, shortened. Two pre-
excitation syndromes exist (1) the Wolff-Parkinson-White syndrome, and (2) the
Lown-Ganong-Levine syndrome.

Wolff-Parkinson-White Syndrome (WPW): Patients with WPW possess an
accessory pathway of depolarization, the bundle of Kent. Three
electrocardiographic criteria for WPW are: (1) a short P-R interval, (2) a wide
QRS complex, and (3) a delta wave.

The QRS complex is widened by the delta wave in exactly the same amount as
the P-R interval is shortened. The delta wave is a slurring of the initial portion of


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the QRS complex produced by early depolarization. The major clinical
manifestation of WPW is recurrent tachycardia.

Lown-Ganong-Levine Syndrome (LGL): LGL is the result of some of the
internodal fibers' (James fibers) bypassing the major portion of the
atrioventricular node and terminating in the bundle of His. The three criteria for
LGL are: (1) a short P-R interval without a delta wave, a) a normal QRS, and (3)
recurrent paroxysmal tachycardia. It should be noted that, unlike in WPW,
episodes of tachycardia are required for the diagnosis of LGL.

Intraventricular Conduction Disturbances

Background: In the normal process of ventricular depolarization, the electrical
stimulus reaches the ventricles by way of the atrioventricular (AV)junction. Then
the depolarization wave spreads to the main mass of the ventricular muscle by
way of the right and left bundle branches. The right bundle branch is undivided,
while the left divides into anterior and posterior fascicles. Normally the entire
process of ventricular depolarization occurs in less than 0.1 seconds. Any
process that interferes with normal depolarization of the ventricles may prolong
the QRS width.

Right Bundle Branch Block (RBBB): Septal depolarization results in a small R
wave in V1. Left ventricular depolarization results in an S wave. Right ventricular
depolarization produces a second R wave. The delayed depolarization of the
right ventricle causes an increased width of the QRS complex to at least 0.12
seconds. Hence, RBBB is characterized by an R-R1 configuration in lead V1 with
a QRS complex > 0.12 seconds. RBBB occasionally can be seen in normal
subjects.

Incomplete RBBB: This shows the same QRS pattern as a complete RBBB;
however, the QRS duration is between 0.1 and 0.12 seconds.

Left Bundle Branch Block (LBBB): Blockage of conduction in the left bundle
branch prior to its bifurcation results primarily in delayed depolarization of the left
ventricle. In LBBB, the septum depolarizes from right to left, since its
depolarization now is initiated by the right bundle branch. Next the right ventricle
depolarizes, followed by delayed depolarization of the left ventricle, giving an R-
R1 configuration in lead V6 and a QRS interval 0.12 seconds. Hence, LBBB is
characterized by an R-R1 configuration in lead V6 and a QRS interval > 0.12
seconds. Unlike RBBB, LBBB always is a sign of organic heart disease.

Incomplete LBBB: This shows the same QRS pattern as a complete LBBB;
however, the QRS duration is between 0.1 and 0.12 seconds.


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Fascicular Blocks (hemi-blocks): These are blockages of transmission that
also may occur in the anterior or posterior branches (fascicles) of the left bundle
branch. The main effect of a fascicular block is to markedly change the QRS axis
without changing the shape or duration of the QRS wave form.

Left Anterior Hemiblock:* This results in left axis deviation (-30 degrees or
more).

Left Posterior Hemiblock:* This results in right axis deviation (+90 degrees or
more).

Ventricular Arrhythmias

Background: Ventricular tissue is capable of spontaneous depolarization. When
this occurs, a premature ventricular contraction (PVC) is initiated. Because the
depolarization wave arises in the myocardium, it usually does not follow the
normal path of ventricular depolarization. Therefore, the QRS complex is
prolonged and bizarre in shape. In addition to PVCs, ectopic ventricular beats
produce ventricular tachycardia and sometimes ventricular fibrillation. Ventricular
escape rhythms also occur.

Premature Ventricular Contractions (PVC): PVCs are premature beats arising
from the ventricles, and are analogous to premature atrial contractions and
premature junctional contractions. PVCs have two major characteristics: (1) they
are premature and arise before the next normal beat is expected (a P wave is not
seen before a PVC), and (2) they are aberrant in appearance. The QRS complex
always is abnormally wide; the T wave and the QRS complex usually point in
opposite directions. The PVC usually is followed by a compensatory pause.
PVCs may be unifocal or multifocal. Unifocal PVCs arise from the same
ventricular site, and as a result have the same appearance on a given ECG lead.
Multifocal PVCs arise from different foci and give rise to different QRS patterns.

Ventricular Tachycardia: This is defined as a run of 3 or more PVCs and may
occur in bursts or paroxysmally. They may be persistent until stopped by
intervention. The heart rate is usually 120 to 200 beats per minute. Ventricular
tachycardia is a life-threatening arrhythmia.

Ventricular Fibrillation: This occurs when ventricles fail to beat in a coordinated
fashion and, instead, twitch asynchronously. The beats are sometimes divided
into coarse and fine rhythms.

Ventricular Escape Beats: A ventricular focus may initiate depolarization when
a faster pacemaker does not control the rate. They occur after a pause in the
regular rhythm. If a higher focus fails to pick up the rhythm, ventricular escape
beats may continue. When this occurs, the rhythm is called idioventricular and
has a rate usually less than 100 beats per minute. The QRS complex is wide and

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bizarre; P waves will not be present. Idioventricular rhythms are usually of short
duration and require no intervention.

Aberrant Ventricular Depolarization: Here the depolarization wave is initiated
above the ventricular level and, because it is premature, reaches the ventricles
when they are in a partially depolarized state, resulting in a wide QRS complex.
The following rules can be used to determine aberrant ventricular depolarization:
(1) the beat is aberrant if a P wave precedes the wide QRS complex, (2) the
preceding R-R interval usually is longer than the other ones, (3) most aberrant
beats are conducted via the left bundle branch, giving the appearance of right
bundle branch block in lead V1, and (4) the initial deflection of the wide QRS is in
the same direction as that of the normal QRS complex.

Determination of Axis

Axis: Defined as the mean vector of ventricular depolarization.

Normal Axis: A mean vector between +90 and 0 degrees.

"Gray Zone": A mean vector between 0 and -30 degrees. Equals normal.

Right Axis Deviation: A mean vector of > +90 degrees.

Left Axis Deviation: A mean vector more negative than -30 degrees.

Determining the axis of the mean vector:

 Check lead aVF.

o if aVF is positive, check lead I

 if lead I is positive, axis is normal.

o if aVF is negative, check lead II.

 if lead II is positive, it is in the gray zone.
 if lead II is negative, there is left axis deviation.



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Atrial Enlargement

Background: To evaluate atrial enlargement, look at the P waves in leads II and
V1. The right atrium generates the left portion of the P wave, the left atrium
generates the right as you view the ECG.

Lead II: Generally parallel to the axis of the atrial depolarization vector force.
Would expect the P wave configuration to be a positive deflection from the
baseline that is symmetric to its return to the baseline.

Lead V1: Generally closest to the atria and perpendicular to the axis of the atrial
depolarization vector force. Would expect first a positive deflection and then a
negative deflection from the baseline, resulting in a sinusoidal curve.

Right Atrial Enlargement: Generates an accentuated left-sided portion of the P
wave.

Left Atrial Enlargement: Results in an accentuated right-sided portion of the P
wave.

Ventricular Hypertrophy

Background: The ECG normally reflects left ventricular depolarization because
left ventricular mass is much greater than right ventricular mass.

Right Ventricular Hypertrophy (RVH): When right ventricular muscle mass
become great enough, it causes alterations in the positivity of the right chest
leads. In the absence of myocardial infarction or right bundle branch block, the
diagnosis of RVH can be made when right axial deviation is present and when R
> S in lead V1 or S > R in lead V6.

Left Ventricular Hypertrophy (LVH): Hypertrophy of the left ventricle causes an
increase in the height and depth of the QRS complexes. LVH is present when the
sum of the S wave in V1 and the R wave in V5 or V6 (whichever is larger) > 35
mm. Accuracy in diagnosing LVH can be improved by considering limb lead
criteria; i.e., if the sum of the R wave in lead I and the S wave in lead III > 25 mm.,
LVH is said to be present when either the chest lead criteria or limb lead criteria
is met.

RVH with Strain (systolic overload): In addition to RVH criteria, T wave
inversion and usually ST segment depression are present in the right chest leads.
(ST segment T wave changes are not present in diastolic overload.)


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LVH with Strain (systolic overload): In addition to criteria for LVH, T wave
inversion and ST segment depression occur in the left chest leads. (ST segment
and T wave changes are not present in diastolic overload.)

Myocardial Ischemia

Background: Due to insufficient oxygen supply to the ventricular muscle. It may
be transient, causing angina pectoris, or more severe, causing the death of a
portion of heart muscle (myocardial infarction).

Subendocardial Ischemia: Produces classic angina and subendocardial
myocardial infarction. Involves the inner layer of ventricular muscle.

Transmural Ischemia: Produces Prinzmetal's angina and transmural myocardial
infarction.

Involves the entire thickness of the ventricular wall.

Classic Angina: Produces transient ST segment depression (except in lead aVR,
which may show reciprocal ST segment elevation). Not all patients with coronary
artery disease show ST segment depression during chest pain.

Prinzmetal's Angina: Atypical angina that occurs at rest or at night and results
in ST segment elevation. Thought to be caused by transient transmural ischemia
due to vasospasm. May occur in individuals with otherwise normal coronary
arteries.

Myocardial Infarction

Transmural Infarction: The infarcted area remain in a depolarized (negative)
state. A normal variant - early repolarization - often occurs in younger individuals
and may be confused with myocardial infarction. With early repolarization,
however, the T wave is distinct from the elevated ST segment, whereas with
myocardial infarction, it is incorporated into it. The loss of positivity in the
infarcted area is responsible for the characteristic Q waves that develop in the
leads exploring the infarcted area. Keep in mind that a normal ECG may exhibit
small Q waves in leads I, V5, and V6 that represent only normal septal
depolarization. Q waves, to be considered diagnostic of acute myocardial
infarction, must (1) have a duration of at least 0.04 seconds or (2) have a depth
equal to 25% or more of the height of the R wave.


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Time sequence of myocardial infarctions: 3 stages:

(1) acute phase-ST segment elevations generally appear within a few minutes
and may last 3 to 4 days. During this period of time, Q waves appear in the leads
showing the ST segment elevations.
(2) evolving phase-ST segments begin returning to their baseline, and the T
waves become inserted.
(3) resolving phase-In the weeks to months that follow, the T waves again return
to the upright position. In most cases, the abnormal Q waves persist for months
or even years.
Localization of Myocardial Infarction: MIs tend to be localized to left
ventricular areas supplied by particular branches of the coronary arteries. They
are described by their locations: anterior, inferior, and posterior.

Anterior Infarction: Subdivided into strictly anterior, anteroseptal, and
anterolateral infarctions.

Strictly Anterior Infarction: Diagnostic changes in V3 and V4.

Anteroseptal Infarction: Results in loss of the normal small septal R waves in
V1 and V2 as well as diagnostic changes in V3 and V4.

Anterolateral Infarction: Results in changes in more laterally situated chest
leads (V5, V6), as well as left lateral limb leads (I, aVL).

Inferior Infarction: Produces changes in the leads that explore the heart from
below: leads II, III, aVF.

Posterior Infarction: Does not generate Q wave formation or ST segment
deviation in the conventional 12-lead ECG since there are no posterior exploring
electrodes. Instead, subtle reciprocal changes in the magnitude of R waves in V1
and V2 may occur. In posterior infarction, the R waves in V1 and V2 become
taller than or equal to the S waves (R/S >1) Unlike RVH, right axis deviation is
not present. ST segment depression also may occur in these leads.

Subendocardial Infarction: Affects only repolarization (ST-T complex) and not
depolarization (QRS complex). Hence, Q waves are not characteristic of
subendocardial infarction. When subendocardial infarction occurs, the ECG may
show persistent ST segment depression instead of the transient depression seen
with classic angina. Persistent T wave inversion without ST segment depression
may occur. The ST-T change slowly returns to normal as the infarction resolves.
ECG findings must be combined with the clinical circumstance and cardiac
enzymes to make the diagnosis of subendocardial infarction.


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Pseudo Infarction Syndromes: LBBB and Wolff-Parkinson-White usually have
significant Q waves. Left ventricular aneurysm after extensive infarction may
show persistent ST segment elevation. Pericarditis may show ST segment
elevation and subsequent T wave inversion; however, there is no Q wave
formation. Patients with idiopathic hypertrophic subaortic stenosis often may
have significant Q waves due to distortion of the normal pattern of depolarization.
Dramatic alterations of ST segments and T waves may occur with increased
intracranial pressure.

Patterns Caused by Drug and Electrolyte Effects

Background: The drugs digitalis and quinidine produce major effects on an ECG
that have considerable clinical significance. Two electrolytes-potassium and
calcium-also produce significant ECG effects.

Digitalis: Changes include modification of the ST-T contour, slowing of AV
conduction, and enhancement of ectopic automaticity. Digitalis may produce
characteristic scooping of the ST-T complex. The ST segment and T wave are
fused together, and it is impossible to tell where one ends and the other begins.
This may occur when digitalis is in the therapeutic range. With toxicity, digitalis
can cause virtually any arrhythmia and all degrees of atrioventricular block.

Quinidine: Increases repolarization time and, hence, prolongs the Q-T interval.
In toxic doses, may widen the QRS complex and cause ST segment depression.

Potassium: Hyperkalemia produces tall, peaked T waves, widening of the QRS
complex, and prolongation of the P-R interval. Hypokalemia produces flattening
of the T waves, which may unmask U waves. T waves may become inverted,
and ST segment depression may occur.

Calcium: Hypercalcemia shortens ventricular repolarization time, resulting in a
shortened Q-T interval. Hypocalcemia prolongs the Q-T interval.

Non-specific ST-T Wave Abnormalities

Background: Non-specific abnormalities of the ST-T wave segment are
diagnosed when the repolarization complex is abnormal but does not indicate a
particular diagnosis. Factors such as temperature, hyperventilation, and anxiety
can influence the ST-T complex.


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Further Study;

http://www.ecglibrary.com/ecghome.html

Normal adult 12-lead ECG

The diagnosis of the normal electrocardiogram is made by excluding any
recognised abnormality. It's description is therefore quite lengthy.

 normal sinus rhythm
o each P wave is followed by a QRS
o P waves normal for the subject
o P wave rate 60 - 100 bpm with <10% variation
 rate <60 = sinus bradycardia


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 rate >100 = sinus tachycardia
 variation >10% = sinus arrhythmia
 normal QRS axis
 normal P waves
o height < 2.5 mm in lead II
o width < 0.11 s in lead II
 for abnormal P waves see right atrial hypertrophy, left atrial
hypertrophy, atrial premature beat, hyperkalaemia
 normal PR interval
o 0.12 to 0.20 s (3 - 5 small squares)
 for short PR segment consider Wolff-Parkinson-White
syndrome or Lown-Ganong-Levine syndrome (other causes
- Duchenne muscular dystrophy, type II glycogen storage
disease (Pompe's), HOCM)
 for long PR interval see first degree heart block and
'trifasicular' block
 normal QRS complex
o < 0.12 s duration (3 small squares)
 for abnormally wide QRS consider right or left bundle branch
block, ventricular rhythm, hyperkalaemia, etc.
o no pathological Q waves
o no evidence of left or right ventricular hypertrophy
 normal QT interval
o Calculate the corrected QT interval (QTc) by dividing the QT
interval by the square root of the preceeding R - R interval. Normal
= 0.42 s.
o Causes of long QT interval
 myocardial infarction, myocarditis, diffuse myocardial
disease
 hypocalcaemia, hypothyrodism
 subarachnoid haemorrhage, intracerebral haemorrhage
 drugs (e.g. sotalol, amiodarone)
 hereditary
 Romano Ward syndrome (autosomal dominant)
 Jervill + Lange Nielson syndrome (autosomal
recessive) associated with sensorineural deafness

 normal ST segment
o no elevation or depression
 causes of elevation include acute MI (e.g. anterior, inferior),
left bundle branch block, normal variants (e.g. athletic heart,
Edeiken pattern, high-take off), acute pericarditis

of 19

 causes of depression include myocardial ischaemia, digoxin
effect, ventricular hypertrophy, acute posterior MI, pulmonary
embolus, left bundle branch block
 normal T wave
 causes of tall T waves include hyperkalaemia, hyperacute
myocardial infarction and left bundle branch block
 causes of small, flattened or inverted T waves are numerous
and include ischaemia, age, race, hyperventilation, anxiety,
drinking iced water, LVH, drugs (e.g. digoxin), pericarditis,
PE, intraventricular conduction delay (e.g. RBBB)and
electrolyte disturbance.
 normal U wave


IVMS-CV-Basic Electrocardiography Notes

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IVMS-CV-Basic Electrocardiography Notes